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You Are What You Eat!
It all shows up in our bones.  Male bones are clearly heavier and rougher than female bones.  All due to mechanical traction of the muscles on the bones.  Hormones and nutrition determine the response of our bones to resistance training.

NUTRITION: How does exercise and nutrition build healthy muscles and bones?

Constant exercise is our best litmus test to survey such internal changes before any clinical laboratory test. On the other side, inadequate food intake can also be monitored by our ability to exercise and can be remedied before long term effects set in. How does exercise survey our bodily performance?

6) EXERCISE: Yet exercise is not about just strengthening this muscle group and that other group. Exercise is a surveillance process of what goes in and out of our body. We intake food and inhale air, but we do not know how good they are until we test and tune up our body by exercise. Even good food would not mean any thing if we do not consume it wisely. Exercise would direct the protein in the ingested food to build healthy muscles. Healthy muscles will burn the excess calories and prevent them from depositing as fat plaques in our arteries. Unblocked arteries means vitalized entire bodily organs. Healthy muscles have to be anchored to strong bones. So, exercise strengthens bones. Healthy, strong bones mean very reliable mineral depot. We knew for so long that our bones are dynamic store of minerals. It delivers and receives minerals every moment in our life to sustain the entire bodily needs. These needs of minerals and other nutrients are directed to the very basic building unit of our human organism: the cell. Each cell requires the flow of certain amounts of nutrients to metabolize its own constituents and a way to discharge its waste products. Having accomplished its vital functions, these basic units would have to rely on two fundamental filters to clear the entire bodily byproducts: the lungs and the kidneys. 

Exercise helps the basic units to obtain its basic demands of nutrients and discharging its byproducts by building the very basic dynamic muscular cells. Exercise also helps the two major filters: Lungs and Kidney by enhancing the breathing muscles and the overall circulation through the kidneys.

I like to imagine that exercise as a buildup of a motorized police force all-over the body whose function is to control traffic of nutrients and byproducts and prevent unwanted deposits. The dynamic nature of the muscle and bone units accomplish the task of mobilization of fluids, and the active biochemical processes in the muscles and bones ensure a constant processing of nutrients. In another words, exercise is surveillance, energy, life, or all together. Walking alone would not target the massive groups of muscle of the shoulder, back, or abdomen. Even the lower leg muscle would not benefit fully of walking. Executing our daily activities would prejudice all groups of muscle that are not used in that sort of activities. Above all, scientifically we have solid information that exercise is a crucial to our health and if practiced in certain way would unleash the tremendous potentials that we human are unaware of.

LIPID METABOLISM

-1- Lipids are an energy source that is double that of carbohydrates (9 Calories/gm)

-2- Stored and used in fasting and starvation if no carbohydrates are available.

-3- Burning fat =oxidation require 20% of carbohydrates’ energy to complete oxidation.

-4- Dietary fats are:

(70%) Triglycerides derived from animal or vegetable foodstuff.

Cholesterol ????

Neutral fat ??????

Phospholipids ????

-5- Pancreatic lipase (from pancreas juice poured at the duodenum) and bile salts (from liver bile) are necessary to digest fat (hydrolyses fat to TG, DG, and MG to Glycerol and fatty acids).

-6- Bile salts emulsify fat and alkalinize medium to activate lipase.

-7- No mouth digestion of fat.

-8- No stomach digestion of fat (acidity block gastric lipase).

-9- Final products of digestion of fat before absorption by the intestines are:

-9-a- Trigycerides (TG) 70% CH2(OCOR1)-CH(OCOR2)-CH2 (OCOR3).

-9-b- Digycerides (DG) CH2(OH)-CH(OCOR2)-CH2 (OCOR3).

-9-c- Monogycerides (MG) CH2(OH)-CH(OH)-CH2 (OCOR3).

-9-d- Fatty acids RxCOOH

TG + DG + MG + FA with choleric acid in intestinal wall } bile salts emulsions

-9-e- Glycerol CH2(OH)-CH(OH)-CH2 (OH).

Water soluble inside intestinal wall.

-9-f- Phospholipids: Pancreatic Phosphatidase (in intestine) + hydrophilic }

hydrolyzed in intestinal wall (emulsifying) into : Glycerol, fatty acids, phosphate base, and nitrogen base

-9-g- Cholesterol: Bile + fatty acid esterifying + pancreatic cholesterol esterase } ester inside wall of intestine.

-9-h- Neutral fat: milky emulsion (chyle)

-10- Circulation:

-10-1- Portal circulation (to liver): Glycerol + FA + Phosphate and nitrogen bases + bile salts.

-10-2- Lymphatic lacteals (thoracic duct to subclavian vein to right heart): Cholesterol + neutral fat

- fat globules in blood after fatty meal (lipemia)

- Plasma lipoprotein lipase (catalyzed by heparin and acidic polysaccharides) hydrolyses it to MG, DG, and FA = clearing factor to be taken by (tissue + heart + lungs + adipose tissues)

-11- Liver: Fat

-11-1- Storage: If excess fatty liver results

-11-1-a- Diabetes mellitus (severe and untreated) excess fat migration and storage

-11-1-b- Starvation

-11-1-c- Lipotropic factors deficiency: Needed for phospholipid formation and plasma protein synthesis

1- Choline

2- Methionine

3- Betaine

4- Inosotol

5- Serine

6- Vitamin B12

-11-1-d- Excess cholesterol in diet

-11-1-e- Pancreatic enzymes lack (trypsin and chymotrypsin)

-11-1-f- Proteolytic enzymes lack (cause decrease methionine)

-11-1-g- Injury to liver: alcohol, poisons

-11-2- Conversion: to phospholipids (easily mixed with blood + easily hydrolyzed by esterases + distributed to tissues + less saturated than neutral fat == active)

-11-3- Degradation: to non esterified fatty acids.

-12- Blood: 570 mg/100 ml lipid plasma (1-3 hr post absorptive)

1- Phosphatides (phospholipids) = 215 mg (lecithin 50-200 mg + cephalin 50-130 mg + sphyngomyelins 15-35 mg).

2- Cholesterol = 200 mg (2/3 esterified with FA + 1/3 free sterols)

3- TG = 142 mg

4- (NEFA) = 12 mg Free non esterified fatt acids (transport fat from depots to liver for oxidation + bound to serum albumin + form lipoprotein)

a) Decrease on administration of (fat, calories = glucose , insulin injection)

b) Increase in Fasting + D.M. + Adrenalin injection + Obesity

-13- Tissue stores of fat (Depots): Chiefly store TG in internal organs and adipose tissues:

-a- Chief energy reserve: 6 kg neutral fat + Carbohydrates: glycogen 500 g in average man

-b- Constant during starvation: cell contents =phospholipids + cholesterol= brain, kidney, lung, heart, spleen

-c- Variable on demand to energy requirements: need hormones to regulate break down to free fatty acids= subcutaneous tissue + abdominal cavity + intramuscular connective tissue + surrounding organs (holding heart and kidneys in place)

-d- Enhancers: Insulin increase fatty acid synthesis increase lipid

-e- Deplete: Glucagon + Adrenalin + Growth hormone + prostaglandins + low fat diet lowering blood essential FA= stimulate lipolysis and activate lipase by cyclic AMP.

FAT BURNING: ENERGY PRODUCTION:

Free fatty acid oxidation in liver, heart, and kidneys need:

- Thiokinase

- Thiophorase

- ATP and Mg++

- Dehydrogenases: Acyl CoA + FAD and beta hydroxy acyl CoA + NAD

- Hydratase

- Thiolase

1) Hydrolysis: Neutral fat is hydrolyzed by LIPASE to = glycerol + fatty acids.

2) Activation: Glycerol is activated by ATP and glycerol KINASE to glycerol-phosphate

Only in Liver and kidney = ATP + alpha glycerokinase

3) Oxidation: Glycerol-phosphate is oxidized by a DEHYDROGENASE + NADH to dihydroxy-acetone Phosphate and produces 3 ATP molecules. Or oxidation glyceraldehydes-3-P

4) Dihydroxy-acetone Phosphate is oxidized to Pyruvic acid and gives 5 ATP and enters citric acid cycle bythe action of acetyl CoA to produce 15 ATP

5) Activation: fatty acids activated in cytoplasm of cells (Liver + Heart + Kidney) by two enzyme sets to combine acetyl CoA by a –S bond:

- Thiokinase + CoA.SH +ATP + Mg++= acetyle CoA synthetase

- Thiophorase + succinyl CoA

6) Carrier to transmit acidic dervative of CoA (SATURATED FATTY ACID) from cytoplasm into mitochondrium: Carnitine Ò - hydroxy, Ó -tri methyl, amino butyric acid.

7) Unsaturation: inside the mitochondria oxidation means removal of 2 hydrogen atoms by FAD (flavoprotein) and Acyl CoA dehydrogenase = produces unsaturated fatty acid and shuttle the hydrogen atoms to the resoiratory chain to produce energy.

8) Hydration of unsaturated fatty acid by enoyl-CoA hydratase produces hydroxy acyl CoA.

9) Second oxidation by NAD and dehydrogenase produces a keto acyl CoA and hydrogen atoms to respiratory chain.

10) Cleavage of 2 carbon atoms by Thiolase+ CoA.SH produces final = fatty acids with 2C less + hydrogen energy to respiratory chain + acetyl CoA enters citric acid cycle.

Thus oxidation of fatty acids means first activation by energy ATP and enzymes then transport into mitochondria, then unsaturating it by oxidation by FAD to remove hydrogen to respiratory chain then hydrating it and oxidating again then cleaving two carbon atoms to produce acetyl CoA. Repeating by oxidation and cleavage of C-atoms produces more acetyl CoA and more energy to the respiratory chain and more acetoacetic acid to ketosis. Thus saturated fats needs more cycles of oxidation and needs more enzymes and catalysts to be burn.

11) The fatty acid with 2C less repeat the cycle of cleavage and degradation.

12) The Acetyl -S.CoA :

- Liver condense 2 molecules to aceto-acetic acid and deliver to blood stream for extrahepatic tissue use where it enters citric acid cycle.

- In liver if oxaloacetic acid from carbohydrates is available, enter citric acid to produce carbon dioxide and energy.

 

 
 
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